Modulations of thalamo-cortical coupling during voluntary movement in patients with essential tremor
Alexandra SteinaiD, Sarah Sure, Markus ButziD, Jan VesperiD, Alfons SchnitzleriD, Jan HirschmanniD
Abstract
The ventral intermediate nucleus of the thalamus (VIM) is the main thalamic hub for processing cerebellar inputs and the main deep brain stimulation target for the treatment of essential tremor (ET). As such, it presumably plays a critical role in motor control. So far, however, this structure has been rarely investigated in humans, and almost all of the existing studies focus on tremor. Here, we set out to study neural oscillations in the VIM and their coupling to cortical oscillations during voluntary movement. We investigated thalamo-cortical coupling by means of simultaneous recordings of thalamic local field potentials and magnetoencephalography in 10 ET patients with externalized deep brain stimulation electrodes. Brain activity was measured while patients were pressing a button repeatedly in response to a visual cue. In a whole-brain analysis of coherence between VIM and cortex, we contrasted activity around a pre-movement baseline and button pressing. Button pressing was associated with a bilateral decrease of thalamic power in the alpha (8- 12 Hz) and beta (13-21 Hz) band and a contralateral power increase in the gamma (35- 90 Hz) band. Moreover, changes in VIM-cortex coherence were observed. Alpha/low beta (8- 20 Hz) coherence decreased before and during movement, and the effect localized to the supplementary motor area and premotor cortex. A rebound of high beta (21-35 Hz) coherence occurred in the same region, but was more focal than the suppression. Pre-movement levels of thalamo-cortex low-beta coherence correlated with reaction time. Our results demonstrate that voluntary movement is associated with modulations of behaviourally relevant thalamic coupling, primarily to premotor areas. We observed a clear distinction between low- and high-beta frequencies and our results suggest that the concept of "antikinetic" beta oscillations, originating from research on Parkinsons disease, is transferable to ET.
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